The influence of steatosis and of other donor and recipient characteristics in affecting liver performance post-orthotopic liver transplantation (OLT) was evaluated in 311 consecutive liver transplantations made in 278 patients. Donor variables considered were age, sex, blood group, cause of death, intensive care unit (ICU) days, need for vasopressors, hepatic enzymes and bilirubin, total and warm ischemia time, and macro- and microvescicular steatosis. Recipient variables considered were age, sex, blood group, biliary output, and post-OLT peak levels of hepatic enzymes. Patient and graft survival were the main outcome indicators. In the multivariate analysis, macrovescicular steatosis involving 25% or more of the hepatocytes was the only variable independently associated with shorter patient survival (p < 0.05). Five (62.5%) of the eight livers with macrovescicular steatosis involving 25% or more of the hepatocytes incurred in a delayed non-function (DNF) and one (12.5%) in a primary non-function (PRNF). The incidence of DNF and PRNF in the group with macrovescicular steatosis involving less than 25% of the liver cells was 1.6% (p < 0.001) and 2.3%, respectively. Microvescicular steatosis of any degree was not associated with a worse prognosis. Macrovescicular steatosis involving 25% or more of the hepatocytes identifies marginal livers, the use of which significantly increases the risk of graft non-function post-OLT.

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Hepatitis C virus (HCV) isHepatitis C virus (HCV) is a major cause of posttransfusion and community-acquired hepatitis in the world (8,24,25). The majority of HCV-infected individuals develop chronic hepatitis that may progress to liver cirrhosis and hepatocellular carcinoma (15). Treatment options for chronic HCV infection are limited, and a vaccine to prevent HCV infection is not available (11,15,17).HCV has been classified in a separate genus (Hepacivirus) of the Flaviviridae family. The virion contains a positive-stranded RNA genome of approximately 9.6 kb in length (25). The genome consists of a highly conserved 5Ј noncoding region followed by a long open reading frame of 9,030 to 9,099 nucleotides that is translated into a single polyprotein of 3,010 to 3,030 amino acids. Processing of the polyprotein occurs by a combination of host and viral proteases. The HCV structural proteins comprise the putative nucleocapsid or core protein and the two envelope glycoproteins E1 and E2 (25). The E2 glycoprotein is thought to be responsible for initiating virus attachment due to its ability to bind to human cells (32).HCV purified from plasma has been reported to exist in association with plasma lipoproteins, suggesting that the virus may use the low-density lipoprotein receptor for uptake (2). In the absence of highly purified native infectious HCV particles as a tool for the study of virus-cell interaction, recombinant HCV glycoprotein E2, E1E2 liposomes (22), infectious HCV pseudotype particles expressing E1 and E2 (HCVpp) (4, 16), and HCV-like particles (HCV-LPs) (3,39,41) have been used to analyze virus-cell membrane interaction. Based on these experimental in vitro studies, CD81 (5, 32), dendritic cellspecific intercellular adhesion molecule 3 grabbing nonintegrin (33) and highly sulfated heparan sulfate (3) have been proposed to play a role in mediating E2 binding and/or HCV internalization.Recently, the scavenger receptor class B type I (SR-BI) has been proposed as a putative HCV receptor candidate (36). SR-BI, a high-density lipoprotein-binding molecule, plays a functional role in lipid metabolism and is highly expressed in hepatocytes and steroidgenic tissues (34). SR-BI is a 509-residue glycoprotein with a large extracellular loop (LEL) anchored to the plasma membrane at both the N and C termini by transmembrane domains with short extensions into the cytoplasm (21). SR-BI has been shown to play a role in mediating the binding of recombinant E2 to HepG2 hepatoma cells and the entry of recombinant HCVpp into Huh-7 hepatoma cells (5, 36). Due to the lack of convenient in vitro or in vivo models for the study of HCV infection, the

Italy was the first Western country to face the COVID-19 pandemic. Here we report the results of a national survey on kidney transplantation activity in February and March 2020, and the results of a three-round Delphi consensus promoted by four scientific societies: the Italian Society of Organ Transplantation, the Italian Society of Nephrology, the Italian Society of Anesthesia and Intensive Care, and the Italian Group on Antimicrobial Stewardship. All 41 Italian transplant centers were invited to express their opinion in the Delphi rounds along with a group of seven experts. The survey revealed that, starting from March 2020, there was a decline in kidney transplantation activity in Italy, especially for living-related transplants. Overall, 60 recipients tested positive for SARS-CoV2 infection, 57 required hospitalization, 17 were admitted to the ICU, and 11 died. The online consensus had high response rates at each round (95.8%, 95.8%, and 89.5%, respectively). Eventually, 27 of 31 proposed statements were approved (87.1%), 12 at the first or second round (38.7%), and 3 at the third (9.7%). Based on the Italian experience, we discuss the reasons for the changes in kidney transplantation activity during the COVID-19 pandemic in Western countries. We also provide working recommendations for the organization and management of kidney transplantation under these conditions.

Hepatitis delta virus (HDV) is a naturally occurring subviral satellite of hepatitis B virus (HBV). 1 The HDV virion is composed of HDV RNA, hepatitis delta antigen (HDAg), and hepatitis B surface antigen (HBsAg), provided as the HBV helper function. Although HDV is able to replicate its RNA within cells in the absence of HBV, 2 HBsAg is required for packaging and release of HDV virions, 3,4 as well as for infectivity. 5 As a result, HDV infects individuals only in association with HBV. Thus, the two commonly described modes of HDV infection are acute coinfection with both viruses and superinfection of HBV carriers with HDV. Acute HBV/HDV coinfection usually resolves, but is more often associated with fulminant hepatitis than is acute HBV infection alone. HDV superinfection of HBV carriers leads to chronic type D hepatitis, which advances to cirrhosis and liver failure more rapidly than viral hepatitis caused by HBV alone. 1 Consequently, although HDV infection affects only a fraction of HBV cases, the resulting acute or chronic liver failure is a relatively more common indication for liver transplantation in Europe as well as North America. 6,7 Curiously, liver transplantation has a better prognosis in patients with terminal cirrhosis caused by HDV than in those with cirrhosis caused by HBV alone. Thus, even though the graft is often reinfected in both cases, HBV/HDV reinfection results in hepatitis and liver disease in only 50% of cases, whereas reinfection with HBV alone is associated with hepatitis in virtually 100% of patients.The patterns of HDV reinfection observed in transplanted livers initially suggested a third mode of HDV infection, which has been referred to as an autonomous, or ''isolated,'' HDV infection. 8 This infection pattern was described in 30% to 60% of transplantation patients who experienced either acute hepatitis type D or intermittent HDV viremia without hepatitis during the follow-up period. 9,10 The peculiar features of the apparently isolated HDV infection were: 1) the detection of HDAg but not HBV antigens in the liver shortly after transplantation, and before either HDV or HBV was detectable in the serum by standard blotting methods; and 2) the detection of HDV in the serum without evidence of HBV DNA or HBsAg by standard blotting and enzyme immunoassay methods. These features differed from the serological patterns observed in either coinfection or superinfection, in